Alpha motor neuron

Alpha (α) motor neurons (also called alpha motoneurons), are large, multipolar lower motor neurons of the brainstem and spinal cord. They innervate extrafusal muscle fibers of skeletal muscle and are directly responsible for initiating their contraction. Alpha motor neurons are distinct from gamma motor neurons, which innervate intrafusal muscle fibers of muscle spindles.

While their cell bodies are found in the central nervous system (CNS), α motor neurons are also considered part of the somatic nervous system—a branch of the peripheral nervous system (PNS)—because their axons extend into the periphery to innervate skeletal muscles.

An alpha motor neuron and the muscle fibers it innervates is a motor unit. A motor neuron pool contains the cell bodies of all the alpha motor neurons involved in contracting a single muscle.

Alpha motor neuron
Alpha motor neurons are derived from the basal plate (basal lamina) of the developing embryo.
NeuroLex IDsao1154704263
Anatomical terms of neuroanatomy


Alpha motor neurons (α-MNs) innervating the head and neck are found in the brainstem; the remaining α-MNs innervate the rest of the body and are found in the spinal cord. There are more α-MNs in the spinal cord than in the brainstem, as the number of α-MNs is directly proportional to the amount of fine motor control in that muscle. For example, the muscles of a single finger have more α-MNs per fiber, and more α-MNs in total, than the muscles of the quadriceps, which allows for finer control of the force a finger applies.

In general, α-MNs on one side of the brainstem or spinal cord innervate muscles on that same side of body. An exception is the trochlear nucleus in the brainstem, which innervates the superior oblique muscle of the eye on the opposite side of the face.


In the brainstem, α-MNs and other neurons reside within clusters of cells called nuclei, some of which contain the cell bodies of neurons belonging to the cranial nerves. Not all cranial nerve nuclei contain α-MNs; those that do are motor nuclei, while others are sensory nuclei. Motor nuclei are found throughout the brainstem—medulla, pons, and midbrain—and for developmental reasons are found near the midline of the brainstem.

Generally, motor nuclei found higher in the brainstem (i.e., more rostral) innervate muscles that are higher on the face. For example, the oculomotor nucleus contains α-MNs that innervate muscles of the eye, and is found in the midbrain, the most rostral brainstem component. By contrast, the hypoglossal nucleus, which contains α-MNs that innervate the tongue, is found in the medulla, the most caudal (i.e., towards the bottom) of the brainstem structures.

Spinal cord

The corticospinal tract is one of the major descending pathways from the brain to the α-MNs of the spinal cord.

In the spinal cord, α-MNs are located within the gray matter that forms the ventral horn. These α-MNs provide the motor component of the spinal nerves that innervate muscles of the body.

Medulla spinalis - Substantia grisea - English
Alpha motor neurons are located in lamina IX according to the Rexed lamina system.

As in the brainstem, higher segments of the spinal cord contain α-MNs that innervate muscles higher on the body. For example, the biceps brachii muscle, a muscle of the arm, is innervated by α-MNs in spinal cord segments C5, C6, and C7, which are found rostrally in the spinal cord. On the other hand, the gastrocnemius muscle, one of the muscles of the leg, is innervated by α-MNs within segments S1 and S2, which are found caudally in the spinal cord.

Alpha motor neurons are located in a specific region of the spinal cord's gray matter. This region is designated lamina IX in the Rexed lamina system, which classifies regions of gray matter based on their cytoarchitecture. Lamina IX is located predominantly in the medial aspect of the ventral horn, although there is some contribution to lamina IX from a collection of motor neurons located more laterally. Like other regions of the spinal cord, cells in this lamina are somatotopically organized, meaning that the position of neurons within the spinal cord is associated with what muscles they innervate. In particular, α-MNs in the medial zone of lamina IX tend to innervate proximal muscles of the body, while those in the lateral zone tend to innervate more distal muscles. There is similar somatotopy associated with α-MNs that innervate flexor and extensor muscles: α-MNs that innervate flexors tend to be located in the dorsal portion of lamina IX; those that innervate extensors tend to be located more ventrally.


Shh structure
Under the influence of the protein sonic hedgehog, shown here, cells of the floor plate of the developing spinal cord differentiate into alpha motor neurons.

Alpha motor neurons originate in the basal plate, the ventral portion of the neural tube in the developing embryo. Sonic hedgehog (Shh) is secreted by the nearby notochord and other ventral structures (e.g., the floor plate), establishing a gradient of highly concentrated Shh in the basal plate and less concentrated Shh in the alar plate. Under the influence of Shh and other factors, some neurons of the basal plate differentiate into α-MNs.

Like other neurons, α-MNs send axonal projections to reach their target extrafusal muscle fibers via axon guidance, a process regulated in part by neurotrophic factors released by target muscle fibers. Neurotrophic factors also ensure that each muscle fiber is innervated by the appropriate number of α-MNs. As with most types of neurons in the nervous system, α-MNs are more numerous in early development than in adulthood. Muscle fibers secrete a limited amount of neurotrophic factors capable of sustaining only a fraction of the α-MNs that initially project to the muscle fiber. Those α-MNs that do not receive sufficient neurotrophic factors will undergo apoptosis, a form of programmed cell death.

Because they innervate many muscles, some clusters of α-MNs receive high concentrations of neurotrophic factors and survive this stage of neuronal pruning. This is true of the α-MNs innervating the upper and lower limbs: these α-MNs form large cell columns that contribute to the cervical and lumbar enlargements of the spinal cord. In addition to receiving neurotrophic factors from muscles, α-MNs also secrete a number of trophic factors to support the muscle fibers they innervate. Reduced levels of trophic factors contributes to the muscle atrophy that follows an α-MN lesion.


Like other neurons, lower motor neurons have both afferent (incoming) and efferent (outgoing) connections. Alpha motor neurons receive input from a number of sources, including upper motor neurons, sensory neurons, and interneurons. The primary output of α-MNs is to extrafusal muscle fibers. This afferent and efferent connectivity is required to achieve coordinated muscle activity.

Afferent input

Selected pathways between upper motor neurons and alpha motor neurons
UMN origin α-MN target Tract name
Cerebral cortex Brainstem Corticonuclear tract
Cerebral cortex Spinal cord Corticospinal tract
Red nucleus Spinal cord Rubrospinal tract
Vestibular nuclei Spinal cord Vestibulospinal tract
Midbrain tectum Spinal cord Tectospinal tract
Reticular formation Spinal cord Reticulospinal tract

Upper motor neurons (UMNs) send input to α-MNs via several pathways, including (but not limited to) the corticonuclear, corticospinal, and rubrospinal tracts. The corticonuclear and corticospinal tracts are commonly encountered in studies of upper and lower motor neuron connectivity in the control of voluntary movements.

The corticonuclear tract is so named because it connects the cerebral cortex to cranial nerve nuclei. (The corticonuclear tract is also called the corticobulbar tract, as the brainstem is sometimes called the "bulb" of the brain.) It is via this pathway that upper motor neurons from the cortex descend from the cortex and synapse on α-MNs of the brainstem. Similarly, UMNs of the cerebral cortex are in direct control of α-MNs of the spinal cord via the lateral and ventral corticospinal tracts.

The sensory input to α-MNs is extensive and has its origin in Golgi tendon organs, muscle spindles, mechanoreceptors, thermoreceptors, and other sensory neurons in the periphery. These connections provide the structure for the neural circuits that underlie reflexes. There are several types of reflex circuits, the simplest of which consists of a single synapse between a sensory neuron and a α-MNs. The knee-jerk reflex is an example of such a monosynaptic reflex.

The most extensive input to α-MNs is from local interneurons, which are the most numerous type of neuron in the spinal cord. Among their many roles, interneurons synapse on α-MNs to create more complex reflex circuitry. One type of interneuron is the Renshaw cell, discussed later.

Efferent output

Alpha motor neurons send fibers that mainly synapse on extrafusal muscle fibers. Other fibers from α-MNs synapse on Renshaw cells, i.e. inhibitory interneurons that synapse on the α-MN and limit its activity in order to prevent muscle damage.


Like other neurons, α-MNs transmit signals as action potentials, rapid changes in electrical activity that propagate from the cell body to the end of the axon. To increase the speed at which action potentials travel, α-MN axons have large diameters and are heavily myelinated by both oligodendrocytes and Schwann cells. Oligodendrocytes myelinate the part of the α-MN axon that lies in the central nervous system (CNS), while Schwann cells myelinate the part that lies in the peripheral nervous system (PNS). The transition between the CNS and PNS occurs at the level of the pia mater, the innermost and most delicate layer of meningeal tissue surrounding components of the CNS.

The axon of an α-MN connects with its extrafusal muscle fiber via a neuromuscular junction, a specialized type of chemical synapse that differs both in structure and function from the chemical synapses that connect neurons to each other. Both types of synapses rely on neurotransmitters to transduce the electrical signal into a chemical signal and back. One way they differ is that synapses between neurons typically use glutamate or GABA as their neurotransmitters, while the neuromuscular junction uses acetylcholine exclusively. Acetylcholine is sensed by nicotinic acetylcholine receptors on extrafusal muscle fibers, causing their contraction.

Like other motor neurons, α-MNs are named after the properties of their axons. Alpha motor neurons have Aα axons, which are large-caliber, heavily myelinated fibers that conduct action potentials rapidly. By contrast, gamma motor neurons have Aγ axons, which are slender, lightly myelinated fibers that conduct less rapidly.

Clinical significance

Poliomyelitis, caused by the poliovirus seen here, is associated with the selective loss of cells within the ventral horn of the spinal cord, where α-MNs are located.

Injury to α-MNs is the most common type of lower motor neuron lesion. Damage may be caused by trauma, ischemia, and infection, among others. In addition, certain diseases are associated with the selective loss of α-MNs. For example, poliomyelitis is caused by a virus that specifically targets and kills motor neurons in the ventral horn of the spinal cord. Amyotropic lateral sclerosis likewise is associated with the selective loss of motor neurons.

Paralysis is one of the most pronounced effects of damage to α-MNs. Because α-MNs provide the only voluntary innervation to extrafusal muscle fibers, losing α-MNs effectively severs the connection between the brainstem and spinal cord and the muscles they innervate. Without this connection, voluntary and involuntary (reflex) muscle control is impossible. Voluntary muscle control is lost because α-MNs relay voluntary signals from upper motor neurons to muscle fibers. Loss of involuntary control results from interruption of reflex circuits such as the tonic stretch reflex. A consequence of reflex interruption is that muscle tone is reduced, resulting in flaccid paresis. Another consequence is the depression of deep tendon reflexes, causing hyporeflexia.

Muscle weakness and atrophy are inevitable consequences of α-MN lesions as well. Because muscle size and strength are related to the extent of their use, denervated muscles are prone to atrophy. A secondary cause of muscle atrophy is that denervated muscles are no longer supplied with trophic factors from the α-MNs that innervate them. Alpha motor neuron lesions also result in abnormal EMG potentials (e.g., fibrillation potentials) and fasciculations, the latter being spontaneous, involuntary muscle contractions.

Diseases that impair signaling between α-MNs and extrafusal muscle fibers, namely diseases of the neuromuscular junction have similar signs to those that occur with α-MN disease. For example, myasthenia gravis is an autoimmune disease that prevents signaling across the neuromuscular junction, which results in functional denervation of muscle.

See also


  • John A. Kiernan (2005). Barr's the Human Nervous System: An Anatomical Viewpoint (8th ed.). Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-7817-5154-3.
  • Duane E. Haines (2004). Neuroanatomy: An Atlas of Structures, Sections, and Systems (6th ed.). Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4677-9.

External links


Amn or AMN may refer to:

Alpha motor neuron (α-MNs), large lower motor neurons of the brainstem and spinal cord

Access Media Network, communications media company

Afghanistan Mission Network, a coalition network for NATO led missions in Afghanistan

Ahli Mangku Negara, a Malaysian honour

Airman, a low-grade enlisted rank in the US armed forces

Al-Masdar News, a multilingual news website

AMN, a TV station in Griffith, New South Wales, Australia

Amn (Forgotten Realms), a fictional country in the Forgotten Realms

Amnionless, gene for a protein necessary for efficient absorption of vitamin B12

Directorate of General Security, Arabic name of former Iraqi intelligence agency

Gratiot Community Airport, Alma, Michigan, US, IATA code

Adrenoleukodystrophy, a rare X-linked genetic disease

Alianţa Moldova Noastră, a former social-liberal political party in Moldova

Anterior grey column

The anterior grey column (also called the anterior cornu, anterior horn of spinal cord or ventral horn) is the front column of grey matter in the spinal cord. It is one of the three grey columns. The anterior grey column contains motor neurons that affect the skeletal muscles while the posterior grey column receives information regarding touch and sensation. The anterior grey column is the column where the cell bodies of alpha motor neurons are located.


An axon (from Greek ἄξων áxōn, axis), or nerve fiber, is a long, slender projection of a nerve cell, or neuron, in vertebrates, that typically conducts electrical impulses known as action potentials away from the nerve cell body. The function of the axon is to transmit information to different neurons, muscles, and glands. In certain sensory neurons (pseudounipolar neurons), such as those for touch and warmth, the axons are called afferent nerve fibers and the electrical impulse travels along these from the periphery to the cell body, and from the cell body to the spinal cord along another branch of the same axon. Axon dysfunction has caused many inherited and acquired neurological disorders which can affect both the peripheral and central neurons. Nerve fibers are classed into three types – group A nerve fibers, group B nerve fibers, and group C nerve fibers. Groups A and B are myelinated, and group C are unmyelinated. These groups include both sensory fibers and motor fibers. Another classification groups only the sensory fibers as Type I, Type II, Type III, and Type IV.

An axon is one of two types of cytoplasmic protrusions from the cell body of a neuron; the other type is a dendrite. Axons are distinguished from dendrites by several features, including shape (dendrites often taper while axons usually maintain a constant radius), length (dendrites are restricted to a small region around the cell body while axons can be much longer), and function (dendrites receive signals whereas axons transmit them). Some types of neurons have no axon and transmit signals from their dendrites. In some species, axons can emanate from dendrites and these are known as axon-carrying dendrites. No neuron ever has more than one axon; however in invertebrates such as insects or leeches the axon sometimes consists of several regions that function more or less independently of each other.Axons are covered by a membrane known as an axolemma; the cytoplasm of an axon is called axoplasm. Most axons branch, in some cases very profusely. The end branches of an axon are called telodendria. The swollen end of a telodendron is known as the axon terminal which joins the dendron or cell body of another neuron forming a synaptic connection. Axons make contact with other cells—usually other neurons but sometimes muscle or gland cells—at junctions called synapses. In some circumstances, the axon of one neuron may form a synapse with the dendrites of the same neuron, resulting in an autapse. At a synapse, the membrane of the axon closely adjoins the membrane of the target cell, and special molecular structures serve to transmit electrical or electrochemical signals across the gap. Some synaptic junctions appear along the length of an axon as it extends—these are called en passant ("in passing") synapses and can be in the hundreds or even the thousands along one axon. Other synapses appear as terminals at the ends of axonal branches.

A single axon, with all its branches taken together, can innervate multiple parts of the brain and generate thousands of synaptic terminals. A bundle of axons make a nerve tract in the central nervous system, and a fascicle in the peripheral nervous system. In placental mammals the largest white matter tract in the brain is the corpus callosum, formed of some 20 million axons in the human brain.

End-plate potential

End plate potentials (EPPs) are the depolarizations of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called "end plates" because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an action potential reaches the axon terminal of a motor neuron, vesicles carrying neurotransmitters (mostly acetylcholine) are exocytosed and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle.

Exercise-associated muscle cramps

Exercise-associated muscle cramps (EAMC) are defined as cramping (painful muscle spasms) during or immediately following exercise. Muscle cramps during exercise are very common, even in elite athletes. EAMC are a common condition that occurs during or after exercise, often during endurance events such as a triathlon or marathon. Although EAMC are extremely common among athletes, the cause is still not fully understood because muscle cramping can occur as a result of many underlying conditions. Elite athletes experience cramping due to paces at higher intensities. The cause of exercise-associated muscle cramps is hypothesized to be due to altered neuromuscular control, dehydration, or electrolyte depletion.

Extrafusal muscle fiber

Extrafusal muscle fibers are the skeletal standard muscle fibers that are innervated by alpha motor neurons and generate tension by contracting, thereby allowing for skeletal movement. They make up the large mass of skeletal muscle tissue and are attached to bone by fibrous tissue extensions (tendons).

Each alpha motor neuron and the extrafusal muscle fibers innervated by it make up a motor unit. The connection between the alpha motor neuron and the extrafusal muscle fiber is a neuromuscular junction, where the neuron's signal, the action potential, is transduced to the muscle fiber by the neurotransmitter acetylcholine.

Extrafusal muscle fibers are not to be confused with intrafusal muscle fibers, which are innervated by sensory nerve endings in central noncontractile parts and by gamma motor neurons in contractile ends and thus serve as a sensory proprioceptor.

Extrafusal muscle fibers can be generated in vitro (in a dish) from pluripotent stem cells through directed differentiation. This allows study of their formation and physiology.

Gamma motor neuron

A gamma motor neuron (γ motor neuron), also called gamma motoneuron, is a type of lower motor neuron that takes part in the process of muscle contraction, and represents about 30% of ( Aγ ) fibers going to the muscle. Like alpha motor neurons, their cell bodies are located in the anterior grey column of the spinal cord. They receive input from the reticular formation of the pons in the brainstem. Their axons are smaller than those of the alpha motor neurons, with a diameter of only 5 μm. Unlike the alpha motor neurons, gamma motor neurons do not directly adjust the lengthening or shortening of muscles. However, their role is important in keeping muscle spindles taut, thereby allowing the continued firing of alpha neurons, leading to muscle contraction. These neurons also play a role in adjusting the sensitivity of muscle spindles.The presence of myelination in gamma motor neurons allows a conduction velocity of 4 to 24 meters per second, significantly faster than with non-myelinated axons but slower than in alpha motor neurons.

Intrafusal muscle fiber

Intrafusal muscle fibers are skeletal muscle fibers that serve as specialized sensory organs (proprioceptors) that detect the amount and rate of change in length of a muscle. They constitute the muscle spindle and are innervated by two axons, one sensory and one motor. Intrafusal muscle fibers are walled off from the rest of the muscle by a collagen sheath. This sheath has a spindle or "fusiform" shape, hence the name "intrafusal".

There are two types of intrafusal muscle fibers: nuclear bag and nuclear chain fibers. They bear two types of sensory ending, known as annulospiral and flower-spray endings. Both ends of these fibers contract but the central region only stretches and does not contract.

They are innervated by gamma motor neurons and beta motor neurons.

It is by the sensory information from these two intrafusal fiber types that an individual is able to judge the position of their muscle, and the rate at which it is changing.

Intrafusal muscle fibers are not to be confused with extrafusal muscle fibers, which contract, generating skeletal movement and are innervated by alpha motor neurons.

Motor pool (neuroscience)

A motor pool consists of all individual motor neurons that innervate a single muscle. Each individual muscle fiber is innervated by only one motor neuron, but one motor neuron may innervate several muscle fibers. This distinction is physiologically significant because the size of a given motor pool determines the activity of the muscle it innervates: for example, muscles responsible for finer movements are innervated by motor pools consisting of higher numbers of individual motor neurons. Motor pools are also distinguished by the different classes of motor neurons that they contain. The size, composition, and anatomical location of each motor pool is tightly controlled by complex developmental pathways.

Motor unit

A motor unit is made up of a motor neuron and the skeletal muscle fibers innervated by that motor neuron's axonal terminals. Groups of motor units often work together to coordinate the contractions of a single muscle; all of the motor units within a muscle are considered a motor pool. The concept was proposed by Charles Scott Sherrington.All muscle fibres in a motor unit are of the same fibre type. When a motor unit is activated, all of its fibres contract. In vertebrates, the force of a muscle contraction is controlled by the number of activated motor units.

The number of muscle fibers within each unit can vary within a particular muscle and even more from muscle to muscle; the muscles that act on the largest body masses have motor units that contain more muscle fibers, whereas smaller muscles contain fewer muscle fibers in each motor unit. For instance, thigh muscles can have a thousand fibers in each unit, while extraocular muscles might have ten. Muscles which possess more motor units (and thus have greater individual motor neuron innervation) are able to control force output more finely.

Motor units are organized slightly differently in invertebrates; each muscle has few motor units (typically less than 10), and each muscle fiber is innervated by multiple neurons, including excitatory and inhibitory neurons. Thus, while in vertebrates the force of contraction of muscles is regulated by how many motor units are activated, in invertebrates it is controlled by regulating the balance between excitatory and inhibitory signals.

Motor unit number estimation

Motor Unit Number Estimation (MUNE) is a technique that uses electromyography to estimate the number of motor units in a muscle.

Muscle spindle

Muscle spindles are stretch receptors within the body of a muscle that primarily detect changes in the length of the muscle. They convey length information to the central nervous system via afferent nerve fibers. This information can be processed by the brain as proprioception. The responses of muscle spindles to changes in length also play an important role in regulating the contraction of muscles, by activating motor neurons via the stretch reflex to resist muscle stretch.

The muscle spindle has both sensory and motor components.

Sensory information conveyed by primary type Ia sensory fibers and secondary type II sensory fibers, which spiral around muscle fibres within the spindle

Motor action by up to a dozen gamma motor neurons and to a lesser extent by one or two beta motor neurons that activate muscle fibres within the spindle.


Narcolepsy is a long-term neurological disorder that involves a decreased ability to regulate sleep-wake cycles. Symptoms include periods of excessive daytime sleepiness that usually last from seconds to minutes and may occur at any time. About 70% of those affected also experience episodes of sudden loss of muscle strength, known as cataplexy. These experiences can be brought on by strong emotions. Less commonly, there may be inability to move or vivid hallucinations while falling asleep or waking up. People with narcolepsy tend to sleep about the same number of hours per day as people without, but the quality of sleep tends to be worse.The exact cause of narcolepsy is unknown, with potentially several causes. In up to 10% of cases, there is a family history of the disorder. Often, those affected have low levels of the neuropeptide orexin, which may be due to an autoimmune disorder. Trauma, infections, toxins or psychological stress may also play a role. Diagnosis is typically based on the symptoms and sleep studies, after ruling out other potential causes. Excessive daytime sleepiness can also be caused by other sleep disorders such as sleep apnea, major depressive disorder, anemia, heart failure, drinking alcohol and not getting enough sleep. Cataplexy may be mistaken for seizures.While there is no cure, a number of lifestyle changes and medications may help. Lifestyle changes include taking regular short naps and sleep hygiene. Medications used include modafinil, sodium oxybate and methylphenidate. While initially effective, tolerance to the benefits may develop over time. Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) may improve cataplexy.About 0.2 to 600 per 100,000 people are affected. The condition often begins in childhood. Men and women are affected equally. Untreated narcolepsy increases the risk of motor vehicle collisions and falls. The term "narcolepsy" is from the French narcolepsie. The French term was first used in 1880 by Jean-Baptiste-Édouard Gélineau, who used the Greek νάρκη (narkē), meaning "numbness", and λῆψις (lepsis) meaning "attack".

Patellar reflex

The patellar reflex or knee-jerk (myotatic) (monosynaptic) (American spelling knee reflex) is a stretch reflex which tests the L2, L3, and L4 segments of the spinal cord.

Reciprocal inhibition

Reciprocal inhibition describes the process of muscles on one side of a joint relaxing to accommodate contraction on the other side of that joint. In some allied health disciplines this is known as reflexive antagonism. Joints are controlled by two opposing sets of muscles, extensors and flexors, which must work in synchrony for smooth movement. When a muscle spindle is stretched and the stretch reflex is activated, the opposing muscle group must be inhibited to prevent it from working against the resulting contraction of the homonymous muscle. This inhibition is accomplished by the actions of an inhibitory interneuron in the spinal cord.

The afferent of the muscle spindle bifurcates in the spinal cord. One branch innervates the alpha motor neuron that causes the homonymous muscle to contract, producing the reflex. The other branch innervates the inhibitory interneuron, which in turn innervates the alpha motor neuron that synapses onto the opposing muscle. Because the interneuron is inhibitory, it prevents the opposing alpha motor neuron from firing, thereby reducing the contraction of the opposing muscle. Without this reciprocal inhibition, both groups of muscles might contract simultaneously and work against each other.

If opposing muscles were to contract at the same time, a muscle tear can occur. This may occur during physical activities, such as running, during which muscles that oppose each other are engaged and disengaged sequentially to produce coordinated movement. Reciprocal inhibition facilitates ease of movement and is a safeguard against injury. However, if a "misfiring" of motor neurons occurs, causing simultaneous contraction of opposing muscles, a tear can occur. For example, if the quadriceps femoris and hamstring contract simultaneously at a high intensity, the stronger muscle (traditionally the quadriceps) overpowers the weaker muscle group (hamstrings). This can result in a common muscular injury known as a pulled hamstring, more accurately called a muscle strain.

"When the central nervous system sends a message to the agonist muscle (muscle causing movement) to contract, the tension in the antagonist muscle (muscle opposing movement) is inhibited by impulses from motor neurons, and thus must simultaneously relax. This neural phenomenon is called reciprocal inhibition."

Taken from Massage Therapy Principles & Practices by Susan Salvo 1999, pg 161

Renshaw cell

Renshaw cells are inhibitory interneurons found in the gray matter of the spinal cord, and are associated in two ways with an alpha motor neuron.

They receive an excitatory collateral from the alpha neuron's axon as they emerge from the motor root, and are thus "kept informed" of how vigorously that neuron is firing.

They send an inhibitory axon to synapse with the cell body of the initial alpha neuron and/or an alpha motor neuron of the same motor pool.In this way, the Renshaw cell action represents a negative feedback mechanism. A Renshaw cell may be supplied by more than one alpha motor neuron collateral and it may synapse on multiple motor neurons.

Spinal interneuron

A spinal interneuron, found in the spinal cord, relays signals between (afferent) sensory neurons, and (efferent) motor neurons. Different classes of spinal interneurons are involved in the process of sensory-motor integration. Most interneurons are found in the grey column, a region of grey matter in the spinal cord.

Stretch reflex

The stretch reflex (myotatic reflex) is a muscle contraction in response to stretching within the muscle. It is a monosynaptic reflex which provides automatic regulation of skeletal muscle length.

When a muscle lengthens, the muscle spindle is stretched and its nerve activity increases. This increases alpha motor neuron activity, causing the muscle fibers to contract and thus resist the stretching. A secondary set of neurons also causes the opposing muscle to relax. The reflex functions to maintain the muscle at a constant length.

Gamma motoneurons regulate how sensitive the stretch reflex is by tightening or relaxing the fibers within the spindle. There are several theories as to what may trigger gamma motoneurons to increase the reflex's sensitivity. For example, alpha-gamma co-activation might keep the spindles taut when a muscle is contracted, preserving stretch reflex sensitivity even as the muscle fibers become shorter. Otherwise the spindles would become slack and the reflex would cease to function.

This reflex has the shortest latency of all spinal reflexes including the Golgi tendon reflex and reflexes mediated by pain and cutaneous receptors.


Tetanus toxin is an extremely potent neurotoxin produced by the vegetative cell of Clostridium tetani in anaerobic conditions, causing tetanus. It has no known function for clostridia in the soil environment where they are normally encountered. It is also called spasmogenic toxin, or TeNT. The LD50 of this toxin has been measured to be approximately 2.5-3 ng/kg, making it second only to botulinum toxin (LD50 2 ng/kg) as the deadliest toxin in the world. However, these tests are conducted solely on mice, which may react to the toxin differently from humans and other animals.

C. tetani also produces the exotoxin tetanolysin, a hemolysin, that causes destruction of tissues.

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